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Evaluating the contribution of genetics and familial shared environment to common disease using the UK Biobank
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Evaluating the contribution of genetics and familial shared environment to common disease using the UK Biobank
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Journal Article
Evaluating the contribution of genetics and familial shared environment to common disease using the UK Biobank
2016
Overview
Albert Tenesa and colleagues report an analysis of the heritability of 12 complex diseases in 1,555,906 individuals from the UK Biobank. They find that SNP heritability explains a higher proportion of estimated heritability when shared familial environmental factors are taken into account.
Genome-wide association studies have detected many loci underlying susceptibility to disease, but most of the genetic factors that contribute to disease susceptibility remain unknown. Here we provide evidence that part of the 'missing heritability' can be explained by an overestimation of heritability. We estimated the heritability of 12 complex human diseases using family history of disease in 1,555,906 individuals of white ancestry from the UK Biobank. Estimates using simple family-based statistical models were inflated on average by ∼47% when compared with those from structural equation modeling (SEM), which specifically accounted for shared familial environmental factors. In addition, heritabilities estimated using SNP data explained an average of 44.2% of the simple family-based estimates across diseases and an average of 57.3% of the SEM-estimated heritabilities, accounting for almost all of the SEM heritability for hypertension. Our results show that both genetics and familial environment make substantial contributions to familial clustering of disease.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ Analysis
/ Animal Genetics and Genomics
/ Cancer
/ Diabetes
/ Female
/ Gene-Environment Interaction
/ Genetic Predisposition to Disease
/ Genetics
/ Genome-wide association studies
/ Genome-Wide Association Study
/ Genomes
/ Heredity
/ Humans
/ Male
/ Methods
/ Polymorphism, Single Nucleotide - genetics
/ Prostate
/ Quantitative Trait, Heritable
/ Siblings
/ Studies
